• Journal of Food Hygiene and Safety
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• v.14 no.2
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• pp.201-215
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• 1999

Limited information is available on the acceptability of Korean MRLs(maximum residue limits) and the health risk based on the pesticide exposure by food intake. The aim of this study was to evaluate TMDI(theoretical maximum daily intake) and EDI(estimated daily intake) for Korean by using MRLs, food intake, residue data, and correction factors, and compare with ADI(acceptable daily intake) in order to estimate the health risk based on the pesticide exposure. The study was performed in three steps. In the frist step, the residual pesticides in each category of food were investigated using the pesticide residue analytical data(1995-96) from officially approved organizations and the analytical data for poultry was adopted from Korean food code method. In the second step, TMDI was estimated from MRLs and food factors, and was compared with ADI. In the third step, the effectiveness of each culinary treatment (washing, peeling, steaming, boiling, and salting) was evaluated and EDI was calculated using pesticide residue data, food factor, and correction factor by treatment. TMDI obtained from MRLs and food intake, and food intake was summed as 1,100.99 g, which was 79.1% of total consumption. The percent ratio of TMDI to ADI for 156 pesticides was mostly below 80% and only 30 pesticides exceeded the ADI. In particular, non-treated EDI from pesticide residue data and food intake was summed up to about 43 $\mu\textrm{g}$/day/capita, and the rank was procymidone(8.6 $\mu\textrm{g}$) > maleic hydrazide(8.2 $\mu\textrm{g}$) > EPN(3.7 $\mu\textrm{g}$) > deltamethrin(3.5 $\mu\textrm{g}$) > cypermethrin(3.0 $\mu\textrm{g}$). The treated EDI calculated from pesticide residue data, food intake, and correction factor by culinary treatment was summed up to 13.7 $\mu\textrm{g}$/day/captia. The percentage of ADI was TMDI(79.74%) > non-treated EDI (0.17%) > treated EDI (0.04%), and the exposure level of Korean population to whole pesticides was below the level to produce health risk. Oncogenic risk of five pesticides used in Korea whose oncogenic potency(Q*) was known were assessed from TMDI and treated EDI. Dietary oncogenic risk for Korean was estimated to be 2.0$\times$10-3 on the basis of TMDI, 8.3$\times$10-7 on the basis of treated EDI. The oncogenic risk from TMDI exceeded the risk level(1$\times$10-6) of EPA, whereas the oncogenic risk from treated EDI and real exposure level lower than that of EPA.

• Korean Journal of Food Science and Technology
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• v.27 no.6
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• pp.871-877
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• 1995

Dietary intake and oncogenic risk of 12 pesticides used in Korea whose oncogenic potency was known were assessed from published data. Dietary oncogenic risk (excess tumor incidence for a 70-year human life span) for Korean population was estimated to be $2.17{\times}10^{-3}$ on the basis of legal maximum residue limit, $4.33{\times}10^5$ on the basis of maximum practical residue level and $5.10{\times}10^{-6}$ on the basis of mean practical residue level of examined pesticides, all of which exceeded the negligible risk standard $1{\times}10^{-6}$ of US EPA. A systematic follow-up study on those oncogenic pesticides should be undertaken in order to mitigate the people's worry about the cancer risk by the abuse of pesticides in food production.

• Genomics & Informatics
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• v.8 no.4
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• pp.194-200
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• 2010

The PIK3CA gene, oncogenic gene located on human chromosome 3q26.3, is an important regulator of cell proliferation, death, motility and invasion. To evaluate the role of PIK3CA gene in the risk of Korean lung cancer, genotypes of the PIK3CA polymorphisms (rs11709323, rs2699895, rs3729679, rs17849074 and rs1356413) were determined in 423 lung cancer patients and 443 normal controls. Statistical analyses revealed that the genotypes and haplotypes in the PIK3CA gene were not significantly associated with the risk of lung cancer in the Korean population, suggesting that these PIK3CA polymorphisms do not contribute to the genetic susceptibility to lung cancer in the Korean population.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8187-8190
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• 2016

Human papillomaviruses (HPVs) are small, non-enveloped, double-stranded DNA viruses that infect epithelial tissues. Specific genotypes of human papillomavirus are the single most common etiological agents of cervical intraepithelial lesions and cervical cancer. Cervical cancer usually arises at squamous metaplastic epithelium of transformation zone (TZ) of the cervix featuring infection with one or more oncogenic or high-risk HPV (HR-HPV) types. A hospital-based study in a rural set up was carried out to understand the association of HR-HPV with squamous intraepithelial lesions (SILs) and cervical cancer. In the present study, HR-HPV was detected in 65.7% of low-grade squamous intraepithelial lesions (LSILs), 84.6% of high-grade squamous intraepithelial lesions (HSILs) and 94% of cervical cancer as compared to 10.7% of controls. The association of HPV infection with SIL and cervical cancer was analyzed with Chi square test (p<0.001). The significant association found confirmed that detection of HR-HPV is a suitable candidate for early identification of cervical precancerous lesions and in the prevention of cervical cancer in India.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7977-7980
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• 2014

This study was undertaken to evaluate the prevalence of significant cervical pathology among women who are high-risk human papillomavirus (HR-HPV)-positive/cytology negative, the most common combination of positive co-tests. The records of 244 women HR-HPV-positive/cytology-negative who had undergone colposcopy at Srinagarind Hospital, Khon Kaen University during January 2010 and April 2014 were reviewed. Mean age was 46.4 years. Of these 224 women, 75 were positive for HPV types 16/18 (33.5%) and 123 were positive for non-16/18 types (54.9%). HR-HPV was not genotyped in the remaining 26 women (11.6%). Prevalence of significant lesions for the entire cohort was 2.4%, and 2.6% and 3.3%, respectively, for those with HPV 16/18 and other oncogenic HPV types. One woman with HPV 16/18 (1.3%) had invasive cervical cancer. Multiparous women were more likely to be infected with HPV 16/18 compared to nulliparous women (36.3% versus 17.6%, respectively). In conclusion, the prevalence of significant cervical lesion among our study population was 2.4%. Multiparous women were more likely to be infected with HPV 16/18 compared to nulliparous women.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.3
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• pp.953-958
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• 2015

Background: Expression of KRT13, FAIM2 and CYP2W1 appears to be influenced by risk habits, thus exploring the associations of these genes in oral squamous cell cancer (OSCC) with risk habits, clinico-pathological parameters and patient survival may be beneficial in identifying relevant biomarkers with different oncogenic pathways. Materials and Methods: cDNAs from 41 OSCC samples with and without risk habits were included in this study. Quantitative real-time PCR was used to analyze KRT13, FAIM2 and CYP2W1 in OSCC. The housekeeping gene (GAPDH) was used as an endogenous control. Results: Of the 41 OSCC samples, KRT13 was down-regulated in 40 samples (97.6%), while FAIM2 and CYP2W1 were down-regulated in 61.0% and 48.8%, respectively. Overall, there were no associations between KRT13, FAIM2 and CYP2W1 expression with risk habits, selected socio-demographic and clinico-pathological parameters and patient survival. Conclusions: Although this study was unable to show significance, there were some tendencies in the associations of KRT13, FAIM2 and CYP2W1 expression in OSCC with selected clinic-pathological parameters and survival.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.16
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• pp.6887-6892
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• 2014

The oncogenic role of human papillomavirus (HPV) in triggering cervical cancer, the second most common cancer in women worldwide, is well established. Romania ranks in first place in Europe in terms of the incidence of cervical cancer. Geographical widespread data on HPV type-distribution are essential for estimating the impact of HPV vaccines and cervical cancer screening programmes. In this study we aimed to identify the prevalence of HPV genotypes and to establish correlations with abnormal cervical cytology among the female population of Brasov County, Romania. A total of 1,000 women aged 17.3-57 years, attending routine cervical examination in the Obstetrics and Gynecology Hospital of Brasov, Romania, and undergoing both cytological examination and HPV genotyping were screened. Infection with 35 different HPV genotypes was detected in 39.6% of cytological specimens. Overall HPV infections were highest in young women under 25 years (p<0.0001), in which cervical cytological abnormalities also reached the highest prevalence. Patients infected by HPV-16 or HPV-18 showed the highest prevalence of cervical cytological abnormalities. Some 48.2% of women with abnormal cytology were infected with high-risk HPV types whereas less than 3% of them were infected only with low-risk HPV types. Our study showed that the prevalence of high-risk HPV infection among Romanian women is higher compared to other studies in other geographic areas. Thus, we consider that in areas where there is an increased prevalence of high-risk HPV infections, HPV genotyping should be performed in all women aged between 18 and 45 years, and Pap test should be performed every 6 months in women with high-risk HPV infection, even those with previous normal cervical cytology.

• Journal of Life Science
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• v.22 no.4
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• pp.538-544
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• 2012

Ethanol is known as being carcinogenic to humans. In addition, the anti-proliferative effects of ethanol have been described for a variety of tissues and cells. In this study, we investigated the anti-proliferative effects of ethanol on various cancer cells, particularly on oncogenic $ras$-transformed or-injected cells. Ethanol treatment inhibited the cell proliferation of normal control cells, but did not suppress the proliferation of various cancer cells and oncogenic $ras$-transformed cells. Furthermore, ethanol treatment did not interfere with DNA synthesis, which was induced by microinjecting the oncogenic $H-Ras^{V12}$ protein. The anti-proliferative effect of ethanol was rescued by antioxidants, such as $N$-acetylcysteine and 4-methlpyrazole. These results suggest that ethanol cytotoxicity is exerted through free radical formation, and that the anti-proliferative action site of ethanol cytotoxicity either lies upstream, or is independent of Ras.

• BMB Reports
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• v.36 no.1
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• pp.138-143
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• 2003

Of many viral causes of human cancer, few are of greater global importance than the hepatitis B virus (HBV). Over 250 million people worldwide are persistently infected with HBV. A significant minority of these develop severe pathologic consequences, including chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Earlier epidemiological evidence suggested a link between chronic HBV infection and HCC. Further, the existence of related animal viruses that induce acute and chronic infections of the liver, and eventually HCC, confirms the concept that HBV belongs to one of the few human oncogenic viruses. Although it is clear that chronic HBV infections are major risk factors, relatively little is understood about how the viral factors contribute to hepatocarcinogenesis. This review will introduce molecular aspects of the viral infection, and highlight recent findings on the viral contribution to hepatocarcinogenesis.

• Biomedical Science Letters
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• v.24 no.3
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• pp.143-149
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• 2018

Excessive exposure to estrogens is the most important risk factor for the development of hormone-sensitive cancers, especially breast cancer. Estrogen stimulates the expression of genes and proteins involved in cell proliferation by binding to estrogen receptor (ER). Another possible mechanism of ER-independent carcinogenicity of estrogens is based on the hydroxylation of estradiol resulting in the formation of catechol estrogens. Catechol estrogen 4-hydroxyestradiol ($4-OHE_2$) is further oxidized to catechol estrogen-3,4-quinones, the major carcinogenic metabolites of estrogens. Evidence increasingly supports the critical role of $4-OHE_2$ in hormonal carcinogenesis via DNA adduct formation or production of reactive oxygen species, which finally contribute to the transformation of normal mammary epithelial cells and the enhanced growth of breast cancer cells. It is also reported that the level of $4-OHE_2$ or its quinones is highly up-regulated in urine or tissues of breast cancer patients. Thus, we highlight the oncogenic roles of $4-OHE_2$ in catechol estrogen-induced breast carcinogenesis.